Essay on Pathophysiology Case Study

Introduction: Having a sound understanding of pathophysiology is imperative for all allied health practitioners within the Australian healthcare system. Pathophysiology is defined to be the functional changes associated with particular diseases (Webster, 2016). Knowledge of pathophysiology and its related mechanisms is essential as it helps with the thorough understanding of certain diseases, its aetiology and its impact on the patient’s day-to-day life (ANZPAC, 2012).

The aim of all healthcare practitioners is to achieve best possible patient-centered results, make ppropriate clinical decisions and problem-solve with the assistance of pathophysiological principles, such as the development and underlying mechanisms of the disease and associated signs and symptoms. This essay aims to examine Mr. Smith’s (aged 63 years old) case using a systematic approach by outlining and relating the various signs and symptoms experienced to the developed differential diagnoses.

Potential diseases will be concisely discussed in regards to the associated pathophysiological mechanisms, blood tests and physical examination results (RCPA, 2015). Furthermore, further diagnostic tests will be outlined to provide sufficient evidence in order to establish and address the top three potential conditions that may be relevant to Mr. Smith. Pathophysiology: Signs and Symptoms Key signs and symptoms indicated in this case can address differential diagnosis which Mr. Smith could be suffering from.

The patient complains about having inflammation around ankle joints bilaterally and indicated suffering from hypertension and diabetes for the last 20years. One explanation for the uncontrolled ankle oedema could be the possible neffectiveness of his hypertension medication (Diabetes. niddk. nih. gov, 2014). Mr. Smith experiences dyspnea (shortness of breath) possibly due to respiratory distress, especially after any physical exertion. His clinical history indicates he is a heavy smoker, who smokes 15 cigarettes per day, causing dyspnea which may be associated with chronic obstructive pulmonary disease; dominantly emphysema (Mall et al. 2008).

Smoking-induced a chronic inflammatory process which encourages the narrowing and thickening of the airways, damaging the bronchioles and adjacent alveoli (Zhang et al. , 014). Emphysema is described by its chronic inflammation and obstructive conducting airflow, consisting of structures of the lungs (Balkissoon et al. , 2011). Smoking is associated with early morbidity and mortality as the chemicals inside affect the mechanisms of the normal human body. Being 63 y/o may contribute to high systolic blood pressure, hypertension and diabetes (Fleg & Strait, 2012).

Old age increases the chance of developing chronic diseases such as ischaemic heart disease and BHF (Ketata et al. , 2012). The patient presents airway obstruction and possible heart complications. Chronic dyspnea on exertion can be linked to many cardiovascular and respiratory problems. Stretch receptors located in the lung’s bronchioles detect changes in lung expansion which causes irritation by certain chemical stimuli such as tobacco from smoking (Barnes et al, 2014). As a result, this change increases shortness of breath.

As he experiences breathlessness even at rest there is obvious obstruction of airflow. Signs of tachycardia indicates a low supply of oxygen in his blood to innervate the lungs. In relation to erythrocytosis, elevated red blood cell count n the haemoglobin thickens the blood causing the abnormal exportation of oxygen as a result of a decrease in oxygen supply at the subcellular level (Shimizu et al. , 2010). As oxygen and nutrient supply are deprived, muscular and skeletal cells lack the potential of producing ATP to generate energy for mechanical movement such as walking hence the fatigue.

This forceful expiration may be the main cause of the shortness of breath, especially during exertion. As described in Mr Smith’s physical complaints, it is evident that the destruction imposed on the elastic fibres in his alveoli, due to smoking, has caused oss support in the lungs that allow for comfortable breathing. However, emphysema is involved in more than just dyspnoea. Coarse inspiratory crackles were heard in Mr. Smith’s lungs during chest auscultation. The causes of these crackles could be from emphysema or chronic bronchitis (Nath et al. 1974). Since the patient has a dry unproductive cough it is unlikely that he is ring from chronic bronchitis, where increased mucous production as a result of inflammation is prevalent (Zhang et al. , 2014). Physical Examination, Blood Tests and Diagnostic Testing: While Mr. Smith’s physical examination confirms COPD, particularly emphysema, his blood work does not do so. Exposure to tobacco smoke causes an inflammatory cascade that ultimately results in alveolar destruction.

The tobacco smoke causes a release of cytokines and proteases causing ECM degradation, epithelial cells undergo necrosis/apoptosis depending on signaling – which usually provide elastic recoil, lose their contractility (Guglin & Verma, 2012). Based on this, if Mr. Smith was suffering from COPD, chronic bronchitis or emphysema, he would be expected to have levels of white blood cells and ESR. However, they fall within the normal range which is an indication that there is no chronic inflammation (Zhang et al. , 2014). Although there is no chronic inflammation, the patient does present with pale skin and faint bluish lips/ tongue.

This could indicate central cyanosis which is caused by low oxygen saturation. The resulting hypoxemia could be caused by a range of conditions from COPD to congenital heart disease (McMullen et al. , 2013). The patient would need to undergo further testing to determine whether or not the reduced arterial oxygen saturation is a result of cardiac or espiratory conditions. First of all, the practitioner would need to keep a track on the patient’s cough and if it has changed or become productive. A sputum sample and further blood tests will be needed to determine if there is any inflammation.

The fact that the patient did not show increased levels of WBC or ESR, 5 weeks after the onset of dyspnoea, does not mean that the inflammation will not occur later. However, perhaps the most important test needed to determine if the patient has COPD, specifically emphysema, a spirometer would have to be used. A spirometer is used to determine if there is any bstruction to the airways as well as its severity (Erdogan et al. , 2013). The main measurement used to identify an obstructive impairment in the airways is the FEV1/FVC ratio.

The presence of dyspnoea is a symptom of many disorders, not just COPD; it could also be a result of BHF (Heart Foundation, 2011). The risk factors BHF (BHF) are mainly hypertension and diabetes. Both these conditions affect cardiac health by placing extra stress on the heart and causing accumulation of plaque artery walls. High blood pressure is a risk factor for atherosclerosis because high ressure in the arteries damages endothelial lining and causes vascular remodeling (Fleg & Strait, 2012) and promotes the formation of atherosclerotic plaques.

These plaques also develop as a result of diabetes. In diabetic cells, that cannot use glucose, have to find an alternative energy source and usually turn to fats and proteins. The body breaks down fat into fatty acids and sends them to the circulation causing elevated cholesterol levels. The excess cholesterol is ingested by macrophages which turn into foam cells and stimulate a cascade that eventually leads to the formation of vulnerable therosclerotic plaques (American Heart Association, 2015).

Atherosclerosis decreases the luminal diameter of the arteries, causing impaired and reduced blood flow which contributes to the onset of BHF (Webster, 2016). Dyspnoea is one of the indications of BHF. The shortness of breath on exertion results from blood backing up in the pulmonary veins because the heart cannot keep up with the supply in the pulmonary veins so fluid leaks back into the lungs (Barnes et al. , 2014). Mr. Smith experienced dyspnoea that woke him in the night. It was relieved when he sat on the edge of his bed and slept with 2-3 illows.

These symptoms indicate orthopnoea which occurs in the supine position which increases venous return from the lower extremities and elevates the diaphragm (Ketata et al. , 2012) causing the feeling of breathlessness and is relieved when the patient is in a semi-seated position ). Another possibility is paroxysmal nocturnal dyspnoea. This condition is more severe than orthopnoea and occurs because of a sudden failure of left ventricular output with an acute rise in pulmonary venous and capillary pressures (Balkissoon et al. , 2014).

However, the atient’s symptoms do not appear as severe as he was able to alleviate the symptoms by sitting upright. Mr Smith has also complained of fatigue, this is another symptom of BHF as the heart has impaired the ability to function as a pump. If the heart is unable to pump enough blood to meet the needs of the body, then the body induces a compensatory mechanism where blood is drawn away from less vital organs (Shimizu et al. , 2010). In Mr Smith’s case, the body would be diverting blood away from muscle beds in the limbs (which could explain the numbness and in his arm and legs) and sending it to the heart and brain.

The heart usually presents with two sounds, S1 and S2. However in BHF patients, a third sound is able to be detected, S3. S1 is caused by the closure of the mitral and tricuspid valve at the start of systole – this is normal and contributes to the ‘lub’ sound of the heart. The S2 sound is caused by the closure of aortic and pulmonic valves and contributes to the ‘dub’ sound. In the elderly, the presence of S3 is abnormal – it represents diastolic filling. Patients of BHF present this third sound because of volume overload and left ventricular systolic dysfunction (Guglin & Verma, 2012).